Caveolin‐1 and CD40L‐CD40‐TRAF interactions in vascular and metabolic disease

Inflammatory and metabolic disease, such as atherosclerosis and obesity, are the main causes of morbidity and mortality in western societies. In this thesis we show that loss of certain cell structures called caveolin-1, which are important in lipid transport, protects against the initiation and progression of atherosclerosis and that hematopoietic specific loss of caveolin-1 leads to an anti-inflammatory state. Furthermore, we establish an important function for the pro-inflammatory CD40L-CD40-TRAF signaling cascade in atherosclerosis as well as in obesity. We provide strong evidence that a precise intervention in Caveolin-1 biology and CD40L-CD40-TRAF signaling harbors the potential to develop new therapeutic agents to treat inflammatory disease.